Interactivist Summer Institute

July 22 - 26, 2003

Copenhagen




Metacognition and Awareness:
The special case of attention deficit and hyperactivity disorder (ADHD)



Hélène Poissant, Ph.D
UQAM, DSÉ, C.P. 8888, Succ. Centre-ville
Montréal, P.Q. Canada, H3C 3P8
tél: 514 987 3000 (ext. 8946)
fax: 514 987 4608
E-mail: poissant.helene@uqam.ca


Abstract


In this paper we look at different kind of evidence: neurobiological, neuropsychological and medical and argue that individuals with ADHD may experience a lack of metacognition. Metacognition relates to the consciousness that individuals have about their own thinking processes and to the ability to have control of those processes (Vygotsky, 1934/1962). As a component of the metacognitive system, metacognitive knowledge may be used in four different ways: (1) a person may know when she/he knows (self-consciousness) or do not know when she/he does not know (secondary ignorance), (2) a person may know what she/he knows, which can help her/him to predict her/his abilities to succeed in a given task and to estimate her/his confidence in the outcome, (3) a person may know what she/he needs to know (Markman, 1977) to fill in her/his lack of information (perception of lack of information) or the inconsistencies in a given information (perception of inconsistencies of information), and finally, (4) a person may know the usefulness of some strategies for dealing with a given task, e.g., self-questioning Brown (1978, 1987). Another more dynamic aspect of metacognition is self-regulation. This relates to experience, feelings, and thoughts that occur during an ongoing cognitive activity (Flavell, 1979). Those experiences give individuals an internal feedback about the efficiency of their mental monitoring. Self-regulation can intervene in a cognitive activity without the person’s awareness. However, in some circumstances, adults, and to a lesser extent children, are able to consciously use rules and strategies to solve a problem. On the other hand, individuals with ADHD show an inability to “stop and think” before acting, regardless of the task or the situation. The three major aspects of ADHD are hyperactivity, impulsiveness, and inattentiveness. Moreover, these features appear early in childhood for most individuals with an onset often before seven years of age and are marked by chronic behaviors lasting at least six months. For reasons that we will expose in this paper, we assume that ADHD children may experience difficulty engaging in a reflexive activity such as metacognition.


Key words (10)
Metacognition and Awareness, Inhibitory processes, Metamemory, Attention and Working Memory, Frontal lobe

Metacognition and Awareness:
The special case of attention deficit and hyperactivity disorder (ADHD)





Neurobiological Evidence

The fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) (American Psychiatric Association, 2000), describes Attention-Deficit/Hyperactivity Disorder (ADHD) as a disorder that includes a list of specific symptoms of inattention (e.g.: forgetful in daily activities; difficulty with organization) and hyperactivity/impulsivity (e.g.: runs about or climbs excessively, talks excessively, difficulty waiting in turn taking situations). Recently, new research in neurobiology and neuropsychology had shift the focus from a behavioral description of ADHD (re: DSM-IV) to a more cognitive perspective.

Among the diverse biological hypotheses regarding the etiology of ADHD, the hypothesis of frontal dysfunction remains strong. The influence of frontal systems on attention, particularly the elements of higher mental control postulated as prefrontal functions, are illustrated through the presentation of a number of syndromes of abnormal mental awareness associated with prefrontal minimal brain damage (Benson, 1991). For example, Ross, Hommer, Breiger, Varley, and Radant’s (1994) study indicates that children with ADHD showed, relative to normal controls, deficits on inhibiting response during a delay period (800-msec). This difficulty to inhibit response in ADHD may be associated with pathology located outside the dorsolateral prefrontal cortex. Research based on brain imaging indicates that areas in the prefrontal lobe, basal ganglia, and striatum are reduced by about 10 percent in size and activity. These areas are thought to be involved in response, attention, and sensitivity to reward. Zametkin, Nordahl, Gross, King, Semple et al. (1990), using a positron emission tomography scanner (PET scan) observed important differences between people who have ADHD and those who do not. In adults with ADHD, the brain areas that control attention used less glucose, which indicates less activity. Another study, conducted by Shue and Douglas (1992), indicates that ADHD children differed significantly from controls on tasks involving motor control and problem solving skills known to be sensitive to frontal lobe dysfunction.

Klorman (1991) using cognitive event-related potentials (ERP) procedure found that children with ADHD make more errors and react more slowly than controls in tests of sustained attention. Coincident with their poor performance, children with ADHD have smaller late positive components of the ERP. Frank, Seiden, and Napolitano (1994), used this technology to discover that children with learning disabilities (LD) with or without ADHD both have smaller P3 wave amplitude compared to normal children when all groups have to perform an auditory task (two-tone discrimination). Frank et al. (1994) concluded that the smaller P3 amplitude in children with LD-ADHD reflects cognitive and processing difficulties, which frequently coexist with ADHD in these children but that are not specifically related to an attention deficit. Robaey, Cansino, Dugas, and Renault (1995), correlated ERP measurements with scores on the Wechler Intelligence Scale for Children Third Edition (WISC-III) and on a Piagetian battery (Cognitive Development Scale for Children) in normal and ADHD children. Amplitudes and latencies of a fronto-central P250 and of the parieto-occipital N250, P350 and P500 were measured concurrently in four categorization tasks derived from the tests. Their results indicated that in hyperactive children there is a negative correlation between P250 amplitude and the children’s verbalize test scores. In addition, latency-based correlations found in normals were lacking in children with ADHD. They concluded that intelligence forms may not refer to the same use of the same processes in ADHD and normals.

In addition, an important area of ADHD research includes investigations of the brain structures. For example, Hynd, Hern, Novey, Eliopulos, Marshall, et al. (1993), employed magnetic resonance imaging (MRI) to investigate the patterns of morphology of the caudate nucleus in normal and ADHD children. Their results indicate that 72.7% of normal children evidenced a left-larger-than-right pattern of asymmetry, whereas 63.6% of the ADHD children had the reverse pattern of asymmetry. This asymmetry was most notable in boys with ADHD. These results may account for the asymmetries observed in neurotransmitter systems implicated in ADHD. Using the same technology, Semrud-Clikeman, Filipek, Biederman, Steingard, Kennedy, et al. (1994), demonstrated that right-handed male subjects with ADHD have significantly smaller posterior corpus callosum regions than the control group. Moreover, these areas may be related to sustained attention deficits, which in turn impact on the development of more advanced level of attention such as self-regulation. Brain asymmetries and developmental changes in specific anatomical structures linked to ADHD are, however, still controversial topics.

Neuropsychological evidence

Now many psychologists speak of ADHD in terms of an “outlier in the spectrum of human neurological variation” rather than merely as a disorder. The symptoms related to ADHD may appear at one time or another in all individuals, but are more persistent or severe in people with ADHD (Barkley, 1990). Such manifestation of the symptoms was sufficient ground for Barkley (1997,1998) to challenge the DSM-IV primary characteristics associated with ADHD: inattention or inconsistent attention, hyperactivity and impulsiveness. ADHD would have more to do with a lost of interest than with a deficit to concentrate. Barkley points to persistence of effort and impulse control rather than in default in the filtering system of attention. For ADHD children, the urge to act is not controlled or inhibited, so that we may consider the child as hyper-responsive rather than hyperactive. By the age of about four, normal children start to develop self-control along with an internalized language while ADHD children seem to fail to do so and have difficulty to provide a delayed answer (see the above study of Ross, Hommer, Breiger, Varley, and Radant, 1994).

Barkley’s neuropsychological theory predicts that children with ADHD will have a poorer working memory than their normal peers. To be able to hold in memory an information, for even a very short period of time, enables the individual to analyze and reflect about this information. The inability to reflect and therefore to wait prevents the child from behaving in a proper way. For the same reason, children with ADHD will find it difficult to hold back their emotions and seem to feel them more intensively than average people. Such difficulties also lead to a lack of objectivity and consequently make goal-directed behavior less likely. Barkley’s theory also predicts that an important part in self-control and reflection, i.e., the internalized language, is impaired in children with ADHD. The ability to hold a thought enables humans to organize information and to elaborate new relations among this information that lead to a deeper understanding. The inability to do so gives the impression that children with ADHD have difficulty to explain things and do not get to the point but rather around the point. According to Barkley (1997), the disorder in response inhibition and executive function associated with ADHD have among consequences an impairment in self-regulation, an impairment in behavior organization toward the future (or planning), and an impairment in social effectiveness.

A meta-analysis conducted by Barkley, Grodzinsky, and DuPaul (1992) reviewing 22 neuropsychological studies of frontal lobe functions in children with ADHD, predominantly hyperactive or predominantly inattentive, indicates that tests of response inhibition reliably distinguished ADHD children from normal children. Their meta-analysis also suggests that both ADHD groups made more omission errors on a Continuous Performance Test and performed more poorly on the word and interference portions of the Stroop Test compared to normals. Both types of ADHD shared similar deficits on some frontal lobe tests while difficulties related to perceptual-motor speed and processing were found only in children with ADHD predominantly inattentive. Thus, these executive function tests may be helpful in the diagnosis of ADHD children and in the comparison with normals.

On the other hand, methylphenidate (MPH) a psychostimulant of the central nervous system is well recognized to improve ADHD symptomatology. There are several advantages from its intake. MPH benefits in children include increase of their compliance to maternal commands (Barkley, 1988), increase in persistence to tasks (Carlson, Pelham, Milich, & Hoza, 1993) an element that we may associate with metacognition (see Metacognitive Functioning section), improvement of their working memory (Tannock, Ickowicz, & Schachar, 1995), improvement of their social behavior with peers and adults as well as academic performance (Klein, 1993), and improvement on the Go-no go test indicating a decrease in the tendency of children with ADHD to make impulsive commission errors (Trommer, Hoeppner, & Zecker, 1991). In addition, there is evidence that implicates the actions of MPH on the frontal lobe region (Kuczenski, Segal, Leith, & Applegate, 1987; Yasushi, 1987). The drug acts as a dopamine agonist and as such increases the level of available dopamine in the system. Dopaminergic neurons are found in areas such as frontal lobe and limbic system, that are involved in the control of problematic behaviors of children (e.g., motor control, impulsiveness). Furthermore, MPH demonstrated significant effects on tests sensitive to frontal lobe dysfunction such as spatial working memory and planning (Elliot, Sahakian, Matthews, Bannerjea, Rimmer, et al., 1997).

Metacognitive functioning and dysfunctioning

According to Brown (1978, 1987), metacognitive knowledge is used in four different ways: (1) individuals may «know when» they know («self-consciousness») or do «not know when» they do not know («secondary ignorance»), (2) individuals may «know what» they know, which can help them to predict their abilities to succeed in a given task and to estimate their confidence in the outcome, (3) individuals may «know what they need » to know (Markman, 1977) to fill in their lack of information («perception of lack of information») or the inconsistencies in a given information («perception of inconsistencies of information»), and finally, (4) individuals «may know the usefulness of strategies» for dealing with a given task.

Contrary to normal metacognitive functioning, metacognitive dysfunctioning involves a problem in the experience or feeling of conscious awareness of one’s own cognitive performance (Shimamura, 1994). Disruptions of metacognition, characterized by cognition without awareness, can take many clinical forms such as memory without awareness (Jacoby & Witherspoon, 1982). The lack of awareness reported in some clinical cases suggests that many cognitive functions may operate without conscious control. This also suggests that cognitive functions have a componential aspect, that is neural circuits operating in parallel with other metacognitive functions (Shimamura, 1994). Thus different metacognitive impairments may involve different neural circuits depending on the type of cognitive functions that is disrupted. This hypothesis seems to be confirmed in some neurological pathologies. For example, it was found that in organic amnesia patients certain aspects of new learning capacity (during a perceptual-motor skill task and a mirror-reading skill task) are preserved even though the patients did not have an awareness of their capacity or did not have a conscious recollection of having engaged in the task before. This phenomena resembles, although in a reverse way, the “know when” component of metacognition (see Brown, 1978), but here patients do not know when they know (a special case of secondary ignorance). For Shimamura (1994), these findings suggest that certain parts of memory capacity, namely its conscious recollection component may be distinct of its unconscious automatic component. See figure 2 for a reinterpretation of Brown’s secondary ignorance concept in the light of the knowing without awareness phenomenon.

The involvement of frontal lobe in feeling-of-knowing and metacognition seems to be confirmed by other studies. For example, Janowsky, Shimamura, and Squire, (1989) found that patients with frontal lesions were impaired in the ability to judge what they had learned. Other clinical observations (in Korsakoff’s patients) indicate an impairment in their feeling-of-knowing accuracy in addition to deficits in encoding, attention and memory for temporal order. According to Shimamura (1994), one possible explanation implies that frontal lobe damage mediates disorders of metamemory (knowledge of one’s memory capabilities and of strategies that can help memory). Deficits in metamemory expressed by failed judgments and decision making is consistent with other disorders related with frontal lobe dysfunctioning. Patients with frontal lobe lesions do not experiment impairment in perception and memory but rather an impairment in the evaluation or integration of these cognitive functions. Thus the metacognitive impairment related to frontal lesions may be due to a failure to make appropriate judgments based on perceptual and semantic knowledge (Shimamura, 1994).

Since we already know from the etiological data that ADHD seems be linked to minimal frontal lobe dysfunction, these findings about the role of frontal lobe in metacognition are the most relevant here. They strengthen our assumption that ADHD children may experienced a deficit in components of metacognition. In accordance with this idea, researchers have already found similarities between the neurochemical definition of ADHD and brain injury and the symptoms that result from each condition. In this overall context, comparisons of neurological data with neuropsychological and metacognitive data of these children should bring useful information in ADHD diagnosis.

Since we know that ADHD children experience a deficit in executive functioning, we may suspect that they also lack of metacognition. Accordingly, these children might not notice the lack of information in a given instruction even at 8 years of age and up. In the present study, we will mainly concentrate on the «knowing-what-we-need-to-know» aspect of metacognitive knowledge.

Method

Subjects

Control group (n = 30, overall mean age = 8.75) originate from a French public school while ADHD group (n=17, overall mean age = 9.06) comes both from a neurological clinic and a special needs school (n=5). All experimental sites were located in the same Montreal suburban region and subjects were all from the same socioeconomic background. A comparison of the mean ages for ADHD and controls was done to check for possible difference. The t-test indicates no significant difference in the means of age (t45 = 0.6048, p = 0.54). Then, all subjects were divided into three age groups (age group 1= 6-7 years of age; age group 2= 8-9 years of age; age group 3= 10-11.5 years of age) along their indentity as Control or ADHD. The school levels of all subjects range from 1st grade to 6th grade. An observation of ages within each school level indicates that ADHD children appear to have a consistent delay when compared with control children (see table 1). This delay seems greater for the older ADHD subjects (age group 3). We found 50 % of ADHD subjects of age group 3 in the 4th grade compare to no control subject (0%) of this same age group for the same school level (4th grade). Moreover, 17% of ADHD subjects compared to 75% of controls are in age group 3 as well as in the 5th grade. Despite these differences, the Wilcoxon test that was conducted to compare school levels in function of the identity of subjects (ADHD Vs control) did not bring any significant relationship.

On the other hand, all subjects were administered the Conner’s Parent Rating Scale (CPRS-48) and the Conner’s Teacher Rating Scale (CTRS-28) to confirm the DSM-IV diagnostics of ADHD made by the neurologist and to screen for other disorders in controls as well. The CTRS-28 is a questionnaire for teachers that contains 28 items distributed in four factors: conduct problems (CP), hyperactivity (H), inattentive-passive (I-P) and hyperactivity index (H-Index). The CPRS-48 is a questionnaire for parents that contains 48 items distributed in six factors: conduct problem (CP), learning problem (LP), psychosomatic (PS), impulsive-hyperactive (I-H), anxiety (A), hyperactivity index (H-Index). The proportions of children with clinically significant scores (clinical score of more than 65) on the CTRS-28 were found to be, for ADHD, of 30%, 30%, 20% and 40% (for CP, H, I-P and H-Index respectively) and of zero for controls on all four factors. The proportions of children with clinically significant scores (clinical score of more than 65) on the CPRS-48 were found to be, for ADHD, of: 38%, 81%, 19, 38%, 19% and 63% (for CP, LP, PS, I-H, A, and H-Index respectively) and for controls of: 3%, 0%, 17%, 0%, 3% and 0% on the same factors. The high percentage of ADHD children with learning difficulties (81%) is consistent with the literature about the comorbitiy of ADHD and LD. As expected, the ADHD children were found to have a higher score on the hyperactivity index of the Conner’s Parent Rating Scale (CPRS-48) (t18.8 = 3.68, p= 0.0016) and on the Conner’s Teacher Rating Scale (CTRS-28) (t9.2 = 6.3591, p= 0.0001) than the normal children.

Perception of lack of information task («knowing-what-we-need-to-know»)

Following Markman (1977)’s procedure, the experimenter (E) gives verbally and individually to each child (C) the instructions regarding the performance of a Magic Trick and a Game of Cards. The instructions were designed to be incomplete. In the first task, E performs, while he describes it, a magic trick in front of C. First, E shows an empty cup, a plate, a penny and a sheet of paper. E makes sure that C sees that the cup is empty. Then, E puts the plate on the empty cup. Then, E wraps the penny in the paper sheet and puts it on the plate. Finally, E makes the wrapped penny slips from the plate into the cup. (In reality, E pretends to wrap the penny, and let it fall on his own lap. Then E puts the unwrapped penny into the cup, without letting the child know about it). C must discover what E had “forgotten ” (to mention how the penny could be find unwrapped into the cup, since it was wrapped in the first place). During the attempt of C to do the Magic Trick, E asks a series of ten questions (10) to help the child discover the missing information. In the Game of Cards, E tells to C that the goal of the game is to accumulate as much as possible “special cards”. At no point in time, E does explain what are those special cards. At the end of the instructions, C must find if the given instructions were complete or not. Then, E starts to play with C. While C is trying to play the game, E asks the same series of questions (10) to help the child. To avoid any learning effect, the two tasks were performed within a two-month interval and in a counterbalanced way (Magic Trick - Game of Cards or Game of Cards - Magic Trick).

Results

Results of ADHD children indicate for the three groups of age, the following means relative to the perception of lack of information task: group 1: (M = 8.67, SD = 1.15; group 2: M = 6.75, SD = 3.25 and group 3: (M = 2.67, SD = 0.98. Results of control children indicate for the three groups of age, the following means: group 1: (M = 5.56, SD = 2.77; group 2: M = 5.39, SD = 2.34 and group 3: (M = 4.67, SD = 2.83. Overall, we can observe that the control group performs slightly better than the ADHD group. That means, controls need fewer questions to find out the missing information in the game instructions. Moreover, controls appear to perform in a more stable manner than ADHD children. A two-factors ANOVA had been used to compare the means. Results indicate a significant interaction between age groups (1-2-3) and identity factors (:ADHD vs control), F (2,41) = 3.24, p = .0493. This result authorizes us to look for two simple effects: comparison of age groups means within each identity and comparison of identity means within each age group. For each group of comparison, we have used the Bonferroni correction that adjusted the significance levels to 0.0083 and to 0.0167 for the comparison of age groups and the comparison of identity respectively. In ADHD children, it was found that age group 3 performs significantly better than age group 2 (p = 0.0057) and than age group 1 (p = 0.0021). However, we didn’t found any age group significant difference for the controls. This indicates that ADHD children gain profit of getting older and make better metacognitive knowledge judgment than their younger peers. This is not the case for controls for their performance is more stable across ages. On the other hand, overall comparison of ADHD and controls on the perception of lack of information task didn’t bring any significant difference. Finally, we found a marginal effect for school level factor, F (5,41) = 2.07, p= 0.0891. All subjects (ADHD and controls) were found to perform better at the sixth grade compared to the 1st and 2nd grades, (1st grade Vs 6th grade, unadjusted t-test = 2.45, p= 0.0189; 2nd grade Vs 6th grade, unadjusted t-test = 2.85, p= 0.0069).

Discussion

Knowing-what-we-need-to -know is an important aspect of metacognitive knowledge. According to Markman, an instanciation of this aspect : the perception of a lack of information in an instruction, is acquired at around the age of 8 (age group 2 in our study) in normal children. In the present study, we have replicated Markman’s procedure with ADHD children to check for an eventual delay in this population. Contrary to our expectations, our results indicate no significant difference between ADHD and control children for all groups of age combined. However, a significant interaction (age group * identity) indicates that ADHD and control subjects did not perform in the same manner across ages. Thus, the apparent delay of ADHD subjects of the younger age group (when compared to controls of the same age group) is progressively fullfilled as ADHD subjects become older. Actually, ADHD children even bypass, although not in a significant way, the controls in the older category of age (10-11.5). In conclusion, differences between metacognitive knowledge of ADHD children and controls appears to be more a matter of how this metacognitive knowledge develops across age than in the difference in the identity of the two groups per se. The ADHD subjects act as if they takes a longer time to reach the normal group performance (see figure 4).

These results may be interpreted in different ways. First, the question of the association between executive function and metacognitive knowledge found by Shimamura (1994) and of the relation between executive function deficits and ADHD will need further investigation. The phenomenon of knowing without awereness (Shimamura) may be linked with a deficit in executive functions in a different way than the phenomenon of not knowing without awareness that we adressed in our study with the Markman’s protocol. Moreover, deficit in executive functions in ADHD children as described by Bakley (1997) includes functions such as : working nonverbal memory, working verbal memory, self-regulation of affect and reconstitution. These functions are quite different, although not incompatible, to the metacognitive knowledge component that we have addressed here. In addition, Barkley’s recent theory implies that the inattentive and the hyperactive/impulsive aspects of the ADHD syndrome may in fact be two separate syndromes. As such, Barkley explains hyperactive/impulsive syndrome mostly in terms of a lack of behavioral inhibition which includes deficits in the four above mentioned executive functions. An a posteriori examination of the medical files indicates that the vast majority of ADHD subjects that were refered to the neurologist were of the Inattentive type (according to the DSM-IV diagnosis). This difference of type : Inattentive Vs hyperactive/impulsive may be responsable for the encountered absence of difference between controls and ADHD children in our study.

Our results call for a closer look at the metacognitive aspects of ADHD, namely metacognitive knowledge and self-regulation in order to achieve a better comprehension of the syndrome. In the near future it will be interesting to focus our investigation in three main area: (1) to compare the metacognitive processes of three subtypes of ADHD: predominantly Inattentive Type (ADHD-I), predominantly Hyperactive-Impulsive Type (ADHD-HI) and Combined Type (ADHD-C); (2) to compare the development of these metacognitive processes in the normal and ADHD children on a long-term follow-up and (3) to assess the potential efficiency of methylphenidate (MPH) on metacognitive achievement in ADHD children. Correlation between metacognitive data and neuropsychological measurements focusing on executive functions such as behavioral inhibition and working memory may also provide useful clues.

References

Achenback, T.M. (1991). Manual for the Child Behavior Checklist and Revised Child Behavior Profile. Burlington, VT : T. M. Achenbach.

American Academy of Child and Adolescent Psychiatry. (1997). Practice parameters for the assessment and treatment of children, adolescents, and adults with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 36(Suppl.), 85S-121S.

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.

Barkley, R. A. (1988). The effects of methylphenidate on the interactions of preschool ADHD children with their mothers. Journal of the American Academy of Child and Adolescent Psychiatry, 27(3), 336-341.

Barkley, R. A. (1990). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment. New York, NY: Guilford.

Barkley, R. A. (1997). ADHD and the nature of self-control. New York, NY: Guilford.

Barkley, R.A.(1998). Attention-Deficit Hyperactivity Disorder. Scientific American, 9, 66-71.

Barkley, R. A., Grodzinsky, G., & DuPaul, G. J. (1992). Frontal lobe functions in attention deficit disorder with and without hyperactivity: A review and research report. Journal of Abnormal Child Psychology, 20, 163-188.

Benson, D. F. (1991). The role of frontal dysfunction in attention deficit hyperactivity disorder. Journal of Child Neurology, 6(Suppl.), S9-S12.

Biederman, J., Faraone, S. V., Keenan, K., Benjamin, J., Krifcher, B., Moore, C., Sprich-Buckminster, S., Ugaglia, K., Jellinek, M. S., Steingard, R., et al. (1992). Further evidence for family-genetic risk factors in attention deficit hyperactivity disorder. Patterns of comorbidity in probands and relatives psychiatrically and pediatrically referred samples. Archives of General Psychiatry, 49, 728-38.

Bouffard-Bouchard, T., & Pinard, A. (1988). Sentiment d’auto-efficacité et exercice des processus d’autorégulation chez des étudiants de niveau collegial [Self-efficacy and self-regulation among college students]. International Journal of Psychology, 23, 409-431.

Bouffard-Bouchard, T., Parent, S., & Larivée, S. (1993). Self-regulation on a concept-formation task among average and gifted students. Journal of Experimental Child Psychology, 56, 115-134.

Brown, A. L. (1978). Knowing when, where and how to remember: A problem of metacognition. In R. Glaser (Ed.), Advances in instructional psychology. Vol. 1. (pp. 76-115). Hillsdale, NJ: Erlbaum.

Brown, A. L. (1987). Metacognition , executive control, self-regulation, and other more mysterious mechanisms. In F. E. Weinert & R. H. Kluwe (Eds.), Metacognition, motivation, and understanding (pp. 65-116). Hillsdale, NJ: Lawrence Erlbaum.

Cadoret, R. J., & Stewart, M. A. (1991). An adoption study of attention deficit/hyperactivity/aggression and their relationship to adult antisocial personality. Comprehensive Psychiatry, 32, 73-82.

Carlson, C. L., Pelham, W. E., Milich, R., & Hoza, B. (1993). ADHD boys' performance and attributions following success and failure: Drug effects and individual differences. Cognitive Therapy and Research, 17, 269-287.

Chandola, C. A., Robling, M. R., Peters, T. J., Melville-Thomas, G., & McGuffin, P. (1992). Pre- and perinatal factors and the risk of subsequent referral for hyperactivity. Journal of Child Psychology,Psychiatry, and Allied Disciplines, 33, 1077-90.

Conners, K.C. (1990). Conner’s Rating Scale. Toronto: Multihealth System.

Elia, J. (1991). Stimulants and antidepressant pharmacokinetics in hyperactive children. Psychopharmacology Bulletin, 27, 411-415.

Elliott, R., Sahakian, B. J., Matthews, K., Bannerjea, A., Rimmer, J., & Robbins, T. W. (1997). Effects of methylphenidate on spatial working memory and planning in healthy young adults. Psychopharmacology, 131, 196-206.

Faraone, S. V., Biederman, J., & Milberger, S. (1994). An exploratory study of ADHD among second-degree relatives of ADHD children. Biological Psychiatry, 35, 398-402.

Faraone, S. V., Biederman, J., Keenan, K., & Tsuang, M. T. (1991). Separation of DSM-III attention deficit disorder and conduct disorder: Evidence from a family-genetic study of American child psychiatric patients. Psychological Medicine, 21, 109-121.

Flavell, J. H. (1979). Metacognition and cognitive monitoring: A new area of cognitive-developmental inquiry. American Psychologist, 34, 906-911

Frank, Y., Seiden, J. A., & Napolitano, B. (1994). Event-related potentials to an “oddball” auditory paradigm in children with learning disabilities with or without attention deficit hyperactivity disorder. Clinical Electroencephalography, 25, 136-141.

Gross-Tsur, V., Shalev, R. S., & Amir, N. (1991). Attention deficit disorder: Association with familial-genetic factors. Pediatric Neurology, 7, 258-261.

Hechtman, L. (1994). Genetic and neurobiological aspects of attention deficit hyperactive disorder: A review. Journal of Psychiatry and Neuroscience, 19, 193-201.

Hynd, G. W., Hern, K. L., Novey, E. S., Eliopulos, D., Marshall, R., Gonzalez, J. J., & Voeller, K. K. (1993). Attention deficit-hyperactivity disorder and asymmetry of the caudate nucleus. Journal of Child Neurology, 8, 339-347.

Jacobvitz, D., Sroufe, L. A., Stewart, M., & Leffer, N. (1990). Treatment of attentional and hyperactivity problems in children with sympathomimetiv drugs: A comprehensive review. Journal of the American Academy of Child and Adolescent Psychiatry, 29, 677-688.

Jacoby , L.L. , Witherspoon D. (1982). Remembering without awareness. Canadian Journal of Psychology, 36(2), 300-324.

Janowsky, J.S. , Shimamura, A.P. , Squire, L.R. (1989). Source memory impairement in patients with frontal lobe lesions. Neuropsychologia, 27, 1043-1056.

Klein, R. G. (1993). Clinical efficacy of methylphenidate in children and adolescents. Encéphale, 19, 89-93.

Klorman, R. (1991). Cognitive event-related potentials in attention deficit disorder. Journal of Learning Disabilities, 24, 130-140.

Kluwe, R.H. (1987). Executive decisions and regulation of problems solving behavior. In F. E. Weinert & R. H. Kluwe (Eds.), Metacognition, motivation, and understanding (pp. 31-63). Hillsdale, NJ: Lawrence Erlbaum.

Kuczenski, R., Segal, D. S., Leith, N. J., & Applegate, C. D. (1987). Effects of amphetamine, methylphenidate, and apomorphine on regional brain serotonin and 5-hydroxyindole acetic acid. Psychopharmacology, 93, 329-335.

Levy, F., Hay, D. A., McStephen, M., Wood, C., & Waldman, I. (1997). Attention-deficit hyperactivity disorder: a category or a continuum? Genetic analysis of a large-scale twin study. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 737-744.

Markman, E. M. (1977). Realizing that you don’t understand: A preliminary investigation. Child Development, 48, 986-992.

Piaget, J. (1928/1969). Judgment and reasoning in the child. London: Routledge & Kegan Paul (Original work published 1928).

Pinard, A. (1989). La conscience psychologique [Psychological conciousness]. Montréal: Presses de l’Université du Québec.

Robaey, P., Cansino, S., Dugas, M., & Renault, B. (1995). A comparative study of ERP correlates of psychometric and piagetian intelligence measures in normal and hyperactive children. Electroencephalography and Clinical Neurophysiology, 96, 56-75.

Ross, R. G., Hommer, D., Breiger, D., Varley, C., & Radant, A. (1994). Eye movement task related to frontal lobe functioning in children with attention deficit disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 869-874.

Schachar, R., & Tannock, R. (1993). Childhood hyperactivity and psychostimulants: A review of extended treatment studies. Journal of Child and Adolescent Psychopharmacology, 3, 81-97.

Semrud-Clikeman, M., Filipek, P. A., Biederman, J., Steingard, R., Kennedy, D., Renshaw, P., & Bekken K. (1994). Attention-deficit hyperactivity disorder: magnetic resonance imaging morphometric analysis of the corpus callosum. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 875-81.

Shimamura, A.P. (1994). Metacognition: Neuropsychological evidence. In J. Metcalfe & A.P. Shimamura (Eds.), Metacognition: Knowing about knowing (pp. 301-328). Cambridge, MA: MIT Press.

Shue, K. L., & Douglas, V. I. (1992). Attention deficit hyperactivity disorder and the frontal lobe syndrome. Brain and Cognition, 20, 104-24.

Tannock, R., Ickowicz, A., & Schachar, R. (1995). Differential effects of methylphenidate on working memory in ADHD children with and without comorbid anxiety. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 886-896.

Trommer, B. L., Hoeppner, J.-A. B., & Zecker, S. G. (1991). The go-no go test in attention deficit disorder is sensitive to methylphenidate. Journal of Child Neurology, 6(Suppl.), S128-S131.

Vygotsky, (1934/1962). Thought and language (E. Hanfman & G. Vakar, Trans.). Cambridge, Massachussett: MIT Press. (Original work published 1934).

Wechsler, D. (1991). Psychologist Corporation. Wechler Intelligence Scale for Children Third Edition (WISC-III). San Antonio: Harcourt Brace and Company.

Yasushi, M. (1987). Frontal lobe: Mental functions and EEG. American Journal of EEG Technology, 27, 91-101.

Zametkin, A. J., Nordahl, T. E., Gross, M., King, A. C., Semple, W. E., Rumsey, J., Hamburger, S., & Cohen, R. M. (1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. New England Journal of Medicine, 323, 1361-1366.

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